Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardio > MSK L16 Pharmacology MSK > Flashcards

MSK L16 Pharmacology MSK Flashcards

1
Q

Drugs used: in RA

A

NSAIDS

DMARDS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

DMARDS role

A
  • Aim to halt or slow the inflammatory joint destruction
  • Slow onset of actions
  • May have little long-term effect on disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Molecular Mechanisms in RA: Highly complex multi-factor mediation of the pathological process

A
  1. Auto-immune response – auto-antibodies and immune complex
  2. T-cell mediated antigen-specific responses
  3. T-cell independent cytokine networks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Molecular Mechanisms in RA: What is certain

A
  1. T cells are a/the major driving force
  2. Nuclear factor (NF) –kB is activated in the synovium and regulates genes involved in inflammation e.g. TNF, IL etc iNOS and COX-2
  3. MAP kinases are activated in rheumatoid tissues – key regulator of cytokine and metalloproteinase production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

NSAIDS

role

A

Symptomatic treatment – block eicosanoid synthese

→ Provides symptomatic relief of pain and stiffness, but do not alter disease progression.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

DMARDS role

A
  1. To prevent erosive damage
  2. If patient intolerance to NSADS
  3. Extra-articular manifestations of RA
  4. Poor response to NSAIDS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

DMARDS MOA

A

Sulphasalazine
Gold (aurothiomalalte and auranofin)
Methotrexate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

DMARDS example

A

B and T cell action blocking bt unclear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Sulphasalazine: Epi

A

Cheap and commonly first choice in UK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Sulphasalazine: Combination of

A

Sulphapyridine combind with salicycate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Sulphasalazine: Hydrolysed by and to

A

By gut bacteria to sulphapyrieine and 5-aminosalicylic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Sulphasalazine: Suphapyridine action

A

Reduces absorption of antigens from colon that may promote joint inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Sulphasalazine: 5-aminosalicyclic acid action

A

Reduces synthesis of inflammatory mediators e.g. eicosanoids and cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Sulphasalazine: Side effects

A
  • GI
  • Reversible decrease in sperm count
  • Sulphonamide idiosyncratic blood dyscrasias (reducetion in WBC and platelet)
  • Analyphylaxis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Gold (aurothiomalate and Auranofin: Possible MOA

A
  1. Inhibit lymphocyte proliferation
  2. Inhibit release and activity of Lysosomal enzymes
  3. Decrease production of toxic O2 metabolites from phagocytes
  4. Inhibit chemotaxis of neutrophils
  5. Inhibit induction of IL-1 and TNF-alpha
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Gold (aurothiomalate and Auranofin: Acts where

A

Binds to tissue proteins and accumulates widely, incuding in synovium of inflamed joints

17
Q

Gold (aurothiomalate and Auranofin: Toxicity

A 
Can be serious: 
1.	blood disorders – agranulocytosis, aplastic anaemia
2.	Skin rashes
3.	Diarrhoea
4.	Glomerulonephritis
Serious toxic effects in 10% of patiens
18
Q

Methotrexate: Action speed

A

Rapid

19
Q

Methotrexate: Use in

A

DMARD for RA and Chrohns

20
Q

Methotrexate: MOA

A

Not via inhibition of dihydrofolatereductase (DHFR) – for DMARD unsure

21
Q

Methotrexate: MOA thoughts

A

Thought to be via inhibition of enzymes involved in purine metabolism:

  1. Accumulation of adenosine
  2. Inhibition of T cell activation
  3. Suppression of adhesion molecule expression by by T-cell
22
Q

Methotrexate
Time to Benefit
Potential for Toxicity
Toxcities to Monitor

A 
1-2 months	
Moderate	
Myelosuppression
Hepatic fibrosis and cirrhosis
Pulmonary infiltrates
23
Q

Hydroxychloquine
Time to Benefit
Potential for Toxicity
Toxcities to Monitor

A

2-6 months
Low
Macular Damage

24
Q

Leflunomide
Time to Benefit
Potential for Toxicity
Toxcities to Monitor

A 
4-12 wks
Low	
Diarrhea
Alopecia
Rash
Headache
Risk of immunosuppression infection
25
Q

Sulfasalazine
Time to Benefit
Potential for Toxicity
Toxcities to Monitor

A

1-3 months
Low
Myelosuppresion

26
Q

Cyclosporin
Time to Benefit
Potential for Toxicity
Toxcities to Monitor

A 
4-8 wks	
High	
Renal insufficiency
Anaemia
Hypertension
27
Q

Gold, oral
Time to Benefit
Potential for Toxicity
Toxcities to Monitor

A

4-6 months
Low
Myelosupression
Proteinuria

28
Q

Gold, parentral
Time to Benefit
Potential for Toxicity
Toxcities to Monitor

A

3-6 months
Moderate
Myelosupression
Proteinuria

29
Q

Azathioprine
Time to Benefit
Potential for Toxicity
Toxcities to Monitor

A 
2-3 months	
Moderate	
Myelosupression
Hepatotoxicity
Lymphoproliferative disorders
30
Q

Minocycline
Time to Benefit
Potential for Toxicity
Toxcities to Monitor

A 
1-3 months	
Low	
Hyperpigmentation
Dizzines
Vaginal yeast infections
31
Q

Corticosteroids and RA: Uses

A
  1. Intra-articular injections of individual joints (e.g. knee)
  2. In active disease short causes of oral prednisolone, can produce a rapid onset before other drugs
32
Q

Corticosteroids and RA: Standard therapy

A

Combination of low-dose glucocorticoids and sulphasalazine/methotrexate

33
Q

Corticosteroids and RA:Mechanisms

A
  • Immunosuppressants (act on cell-mediated immune responses)

* Decrease transcription of IL-2, TNF-alpha, interferon-y

34
Q

Gout →Acute arthritis

A

Due to deposition of urate crystals in the synovial tissue – very painful

35
Q

Gout →Metabolic disorder

A

Plasma urate concentration increased due to overproduction of purines and/or impaired excretion of purines
→ Seen with poor renal degradation
→ High red meat diet
→ Mostly genetic

36
Q

Gout →Pathology

A
  1. Crystal deposition leads to kinin release/generation of LTB4
  2. Phagocytic neutrophil accumulation
  3. Free radical formation
  4. Call damage and lysis
37
Q

Gout → Treatment

A

Inhibit uric acid synthesis
Increase uric acid secretion (uricosuric drugs)
Inhibit inflammatory cell migration into joints
Give anti-inflammation/analgesic drugs (NSAIDs)

38
Q

Gout →Drugs for Gout

A

Allopurinol → blocks formation of uric acid
Colchicine → inhibits leckocyte migration into joints
Acute → NSAIDS not Aspirin

Cardio (108 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions